{"title":"p16预防途径:衰老作为tau介导的神经退行性变的驱动因素。","authors":"Jeff Y L Lam, Kai Wang, Guojun Bu","doi":"10.1016/j.neuron.2025.06.024","DOIUrl":null,"url":null,"abstract":"<p><p>In this issue of Neuron, Graves et al.<sup>1</sup> report that genetically reducing senescent cells by deleting p16 in a tauopathy mouse model significantly lessens tau pathology, neurovascular dysfunction, and behavioral deficits. Their study highlights the crucial role of p16-dependent senescence in microglia and endothelial cells as active drivers of neurodegeneration.</p>","PeriodicalId":19313,"journal":{"name":"Neuron","volume":"113 14","pages":"2215-2217"},"PeriodicalIF":15.0000,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A p16 pathway to prevention: Senescence as a driver of tau-mediated neurodegeneration.\",\"authors\":\"Jeff Y L Lam, Kai Wang, Guojun Bu\",\"doi\":\"10.1016/j.neuron.2025.06.024\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>In this issue of Neuron, Graves et al.<sup>1</sup> report that genetically reducing senescent cells by deleting p16 in a tauopathy mouse model significantly lessens tau pathology, neurovascular dysfunction, and behavioral deficits. Their study highlights the crucial role of p16-dependent senescence in microglia and endothelial cells as active drivers of neurodegeneration.</p>\",\"PeriodicalId\":19313,\"journal\":{\"name\":\"Neuron\",\"volume\":\"113 14\",\"pages\":\"2215-2217\"},\"PeriodicalIF\":15.0000,\"publicationDate\":\"2025-07-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuron\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.neuron.2025.06.024\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuron","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.neuron.2025.06.024","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
A p16 pathway to prevention: Senescence as a driver of tau-mediated neurodegeneration.
In this issue of Neuron, Graves et al.1 report that genetically reducing senescent cells by deleting p16 in a tauopathy mouse model significantly lessens tau pathology, neurovascular dysfunction, and behavioral deficits. Their study highlights the crucial role of p16-dependent senescence in microglia and endothelial cells as active drivers of neurodegeneration.
期刊介绍:
Established as a highly influential journal in neuroscience, Neuron is widely relied upon in the field. The editors adopt interdisciplinary strategies, integrating biophysical, cellular, developmental, and molecular approaches alongside a systems approach to sensory, motor, and higher-order cognitive functions. Serving as a premier intellectual forum, Neuron holds a prominent position in the entire neuroscience community.